Plant Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Microbiol Spectr. 2023 Jun 15;11(3):e0445722. doi: 10.1128/spectrum.04457-22. Epub 2023 Apr 4.
Burkholderia gladioli strain NGJ1 exhibits mycophagous activity on a broad range of fungi, including Rhizoctonia solani, a devastating plant pathogen. Here, we demonstrate that the nicotinic acid (NA) catabolic pathway in NGJ1 is required for mycophagy. NGJ1 is auxotrophic to NA and it potentially senses R. solani as a NA source. Mutation in the and genes involved in NA catabolism renders defects in mycophagy and the mutant bacteria are unable to utilize R. solani extract as the sole nutrient source. As supplementation of NA, but not FA (fumaric acid, the end product of NA catabolism) restores the mycophagous ability of ΔΔ mutants, we anticipate that NA is not required as a carbon source for the bacterium during mycophagy. Notably, , a MarR-type of transcriptional regulator that functions as a negative regulator of the NA catabolic pathway is upregulated in Δ/Δ mutant and upon NA supplementation the expression is reduced to the basal level in both the mutants. The Δ mutant produces excessive biofilm and is completely defective in swimming motility. On the other hand, Δ/Δ mutants are compromised in swimming motility as well as biofilm formation, potentially due to the upregulation of . Our data suggest that a defect in NA catabolism alters the NA pool in the bacterium and upregulates which in turn suppresses bacterial motility as well as biofilm formation, leading to mycophagy defects. Mycophagy is an important trait through which certain bacteria forage over fungal mycelia and utilize fungal biomass as a nutrient source to thrive in hostile environments. The present study emphasizes that nicotinic acid (NA) is important for bacterial motility and biofilm formation during mycophagy by Burkholderia gladioli strain NGJ1. Defects in NA catabolism potentially alter the cellular NA pool, upregulate the expression of , a negative regulator of biofilm, and therefore suppress bacterial motility as well as biofilm formation, leading to mycophagy defects.
多粘类芽孢杆菌 NGJ1 对包括毁灭性植物病原体茄病镰刀菌在内的多种真菌具有噬真菌活性。在这里，我们证明了 NGJ1 中的烟酸 (NA) 分解代谢途径是噬真菌所必需的。NGJ1 对 NA 是营养缺陷型的，并且它可能将茄病镰刀菌识别为 NA 来源。参与 NA 分解代谢的 和 基因的突变导致噬真菌缺陷，并且突变细菌无法利用茄病镰刀菌提取物作为唯一营养源。由于 NA 的补充，而不是 FA（富马酸，NA 分解代谢的终产物）恢复了 ΔΔ 突变体的噬真菌能力，我们预计在噬真菌过程中 NA 不是细菌所必需的碳源。值得注意的是， 作为 NA 分解代谢途径的负调控因子的 MarR 型转录调节因子在 Δ/Δ 突变体中上调，并且在 NA 补充时，两个突变体中的 表达均降低到基础水平。Δ 突变体产生过多的生物膜，并且在游泳运动中完全缺陷。另一方面，Δ/Δ 突变体在游泳运动和生物膜形成方面都受到影响，这可能是由于 的上调。我们的数据表明，NA 分解代谢的缺陷会改变细菌中的 NA 池，并上调 ，从而抑制细菌运动和生物膜形成，导致噬真菌缺陷。噬真菌是某些细菌在真菌菌丝上觅食并利用真菌生物质作为营养源在恶劣环境中茁壮成长的重要特征。本研究强调了烟酸 (NA) 在多粘类芽孢杆菌 NGJ1 的噬真菌过程中对细菌运动和生物膜形成的重要性。NA 分解代谢的缺陷可能会改变细胞内的 NA 池，上调生物膜的负调控因子 的表达，从而抑制细菌运动和生物膜形成，导致噬真菌缺陷。
